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accession-icon GSE17385
Gene expression profiling from MM1.S cells with control or beta-catenin knockdown.
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

MM1.S cells stably transduced with control or b-catenin shRNA were established. Total RNA was isolated from 5x 10^6 cells of each in triplicate.

Publication Title

Aurora kinase A is a target of Wnt/beta-catenin involved in multiple myeloma disease progression.

Sample Metadata Fields

Cell line

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accession-icon SRP177951
RNAseq for finding splicing events in Arabidopsis prefoldin and lsm8 mutants in different environmental conditions
  • organism-icon Arabidopsis thaliana
  • sample-icon 26 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

This GEO submission includes RNAseq raw data (fastq) and processed data (using ASpli 1.6.0) from samples obtained in the wild type and the single prefoldin4 and lsm8 mutants in three different environmental conditions as well as in the triple prefoldin2 prefoldin4 prefoldin6 mutant growth in standard conditions. Overall design: 28 biological samples from 10 different conditions and genopypes, including the Col-0 WT in each condition (standard, cold and salt conditions)

Publication Title

Prefoldins contribute to maintaining the levels of the spliceosome LSM2-8 complex through Hsp90 in Arabidopsis.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE33143
Targeted disruption of the BCL9/beta-catenin complex in cancer
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Stabilized Alpha-Helix peptides of BCL9 HD2 (SAH-BCL9) block BCL9 and B9L interactions with beta-catenin and specifically downregulate Wnt target gene expression.

Publication Title

Targeted disruption of the BCL9/β-catenin complex inhibits oncogenic Wnt signaling.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE6980
The Differentiation and Stress Response Factor, XBP-1, Drives Multiple Myeloma Pathogenesis
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Multiple myeloma (MM) evolves from highly prevalent premalignant condition termed Monoclonal Gammopathy of Undetermined Significance (MGUS). We report an MGUS-MM phenotype arising in transgenic mice with Emu-directed expression of the unfolded protein/ER stress response and plasma cell development spliced isoform factor XBP-1s. Emu-XBP-1s elicited elevated serum Ig and IL-6 levels, skin alterations and with advancing age, a significant proportion of Emu-xbp-1s transgenic mice develop features diagnostic of human MM including bone lytic lesions. Transcriptional profiles of Emu-xbp-1s B lymphoid and MM cells show aberrant expression of genes known to be dysregulated in human MM including Cyclin D1, MAF, MAFB, and APRIL. This genetic model coupled with documented frequent XBP-1s overexpression in human MM serve to implicate chronic XBP-1s dysregulation in the development of this common and lethal malignancy.

Publication Title

The differentiation and stress response factor XBP-1 drives multiple myeloma pathogenesis.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP032317
Genomic and Proteomic Analyses of Prdm5 Reveal Interactions with Insulator Binding Proteins in Embryonic Stem Cells (RNA-seq)
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II

Description

PRDM proteins belong to the SET domain protein family, which is involved in the regulation of gene expression. Although few PRDM members possess histone methyltransferase activity, the molecular mechanisms by which the other members exert transcriptional regulation remain to be delineated. In this study, we find that Prdm5 is highly expressed in mouse embryonic stem (mES) cells and exploit this cellular system to characterize molecular functions of Prdm5. By combining proteomics and next-generation sequencing technologies, we identify Prdm5 interaction partners and genomic occupancy. We demonstrate that although Prdm5 is dispensable for mES cell maintenance, it directly targets genomic regions involved in early embryonic development and affects the expression of a subset of developmental regulators during cell differentiation. Importantly, Prdm5 interacts with Ctcf, cohesin, and TFIIIC and cooccupies genomic loci. In summary, our data indicate how Prdm5 modulates transcription by interacting with factors involved in genome organization in mouse embryonic stem cells. Overall design: For each condition (ATRA-induced differentiation model and LIF cytokine deprivation) three replicate are available for both Prdm5 wt mES cells and Prdm5 KO mES cells, for a total of 12 samples

Publication Title

Genomic and proteomic analyses of Prdm5 reveal interactions with insulator binding proteins in embryonic stem cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE8498
The MicroRNA miR-124 Promotes Neuronal Differentiation by Triggering Brain-Specific Alternative Pre-mRNA Splicing
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Both microRNAs and alternative pre-mRNA splicing have been implicated in the development of the nervous system (NS), but functional interactions between these two pathways are poorly understood. We demonstrate that the neuron-specific microRNA miR-124a directly targets PTBP1/PTB/hnRNPI mRNA, which encodes a global repressor of alternative pre-mRNA splicing in non-neuronal cells. Among the targets of PTBP1 is a critical cassette exon in the pre-mRNA of PTBP2/nPTB/brPTB, an NS-enriched PTBP1 homolog. When this exon is skipped, PTBP2 mRNA is subject to nonsense-mediated decay. During neuronal differentiation, miR-124a reduces PTBP1 levels leading to the accumulation of correctly spliced PTBP2 mRNA and a dramatic increase in PTBP2 protein. These events culminate in the transition from non-NS to NS-specific alternative splicing patterns. We also present evidence that miR-124a plays a key role in the differentiation of progenitor cells to mature neurons. Thus, miR-124a promotes NS development at least in part by regulating an intricate network of NS-specific alternative splicing.

Publication Title

The MicroRNA miR-124 promotes neuronal differentiation by triggering brain-specific alternative pre-mRNA splicing.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE46821
Prdm5 suppresses ApcMin-driven intestinal adenomas and regulates monoacylglycerol lipase expression
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

PRDM proteins are tissue specific transcription factors often deregulated in diseases, particularly in cancer where different members have been found to act as oncogenes or tumor suppressors. PRDM5 is a poorly characterized member of the PRDM family for which several studies have reported a high frequency of promoter hypermethylation in cancers of gastrointestinal origin. We report here the characterization of Prdm5 knockout mice in the context of intestinal carcinogenesis. We demonstrate that loss of Prdm5 increases the number of adenomas throughout the murine small intestine on an ApcMin background. By genome-wide ChIP-seq and transcriptome analyses we identify loci encoding proteins involved in metabolic processes as prominent PRDM5 targets and characterize monoacylglycerol lipase (Mgll) as a direct PRDM5 target in human colon cancer cells and in Prdm5 mutant mouse intestines. Moreover, we report the downregulation of PRDM5 protein expression in human colon neoplastic lesions. In summary, our data provide the first causal link between Prdm5 loss and intestinal carcinogenesis and uncover an extensive and novel PRDM5 target repertoire likely facilitating the tumor suppressive functions of PRDM5.

Publication Title

Prdm5 suppresses Apc(Min)-driven intestinal adenomas and regulates monoacylglycerol lipase expression.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE142262
MiR-210 impact on the transcriptome suggests regulation of inflammation and regeneration pathways
  • organism-icon Mus musculus
  • sample-icon 22 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

In order to understand the consequences of miR-210 blocking on the ischemia response, the transcriptomic changes were investigated by microarray technology in gastrocnemius muscles of ANTI-210 and SCR treated mice, 7 days after ischemia.

Publication Title

Hypoxia-Induced miR-210 Is Necessary for Vascular Regeneration upon Acute Limb Ischemia.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE20286
Gene expression profiles induced by knockdown and overexpression of p63 variants in MCF-10A mammary epithelial cell line
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

p63 is critical for epithelial development yet little is known about the transcriptional programmes it regulates. The p63 transactivating (TA) isoforms contain an amino-terminal exon that encodes a p53-like transactivation domain, whereas N-isoforms lack this domain but contain the common DNA binding domain (DBD), suggesting that TAp63 and Np63 isoforms may have opposing functions. By characterising transcriptional changes and cellular effects following modulation of p63 expression, we have defined a vital role for p63 in cellular adhesion. Knockdown of p63 expression caused downregulation of cell adhesion-associated genes, cell detachment and anoikis in mammary epithelial cells and keratinocytes. Conversely, overexpression of the TAp63 or Np63 isoforms of p63 upregulated cell adhesion molecules, increased cellular adhesion and conferred resistance to anoikis.

Publication Title

p63 regulates an adhesion programme and cell survival in epithelial cells.

Sample Metadata Fields

Cell line

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accession-icon GSE94867
Impact of short-term high fat diet regimen on hepatic transcriptome
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

We used microarrays to unveil the gene expression alterations upon short-term HFD administration

Publication Title

Dietary alterations modulate susceptibility to Plasmodium infection.

Sample Metadata Fields

Specimen part

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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Developed by the Childhood Cancer Data Lab

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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